The arteriolar injury in hypertension

Gu, Qian; Li, Yang Yang; Chen, Guo Rong; Quinn, MJ

doi:10.1016/j.mehy.2017.12.025

Cited by 2 publications

(2 citation statements)

References 9 publications

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“…In adult hypertension we observe similar lesions in most visceral circulations including kidney, spleen, adrenal, pancreas and liver to those in the uterus (Figure 1b) though it is only the uterine neurovascular lesion that appears to stain positive for P2X3, purinergic receptors (Figure 1c) [32,33]. Visceral arteriolar stenosis was originally described by Drs Alan Moritz and Mary Oldt in Cleveland, OH, in 1937 [34] though its origins in injuries to vasomotor nerves have only recently been described [32,33]. Injuries to visceral, vasomotor nerves release cytokines and growth factors that act on denervated arteriolar walls to produce mural hyperplasia and arteriolar stenosis in similar fashion to that in the uterus and umbilical cord.…”

Section: Postpartum Hypertensionmentioning

confidence: 55%

Pre-eclampsia: the uterine denervation view. Injuries to uterine nerves, the uterorenal “reflex”, and, renal cortico-medullary shunt

Yang¹,

Xin²,

Qing³

et al. 2019

Clin Obstet Gynecol Reprod Med

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Combining two sets of classic, physiologic studies published between 1945 and 1953, with some recent observations, offers a new view of pre-eclampsia (the "uterine denervation" view). In 1945, Dr AT Hertig, (Boston, MA) described narrowing of uterine spiral arterioles, associated with irregular hyperplasia of their vessel walls in the placental bed of women with pre-eclampsia. His illustrations show a "halo" of hyalinised cells around the injured arterioles that has been largely undiscussed in the literature. In many gynecologic syndromes, concentric layers of abnormal, injured nerves surround similarly-narrowed arterioles. There is no "halo" of injured nerves in the "obstetric lesion" because the injured nerves, unlike the narrowed spiral arterioles, cannot extend to the placental bed in pregnancy.In 1953, KJ Franklin and GJ Sophian (London, UK) published results of experiments distending balloons in rabbit uteri where they observed immediate blanching of the kidneys followed by oliguria. Denervating the kidneys abolished the "uterorenal reflex"; persistent distension of the uterus led to acute renal failure. These experiments demonstrated direct neural connections between the uterus and kidneys that caused redistribution of blood flow from the renal cortex to the medulla that have been confirmed in a series of contemporary renal, Doppler studies.The "uterine denervation" view of preeclampsia proposes that stretching injured myometrium and arterioles expressing "new" purinergic (P2X3) "stretch" receptors, activates the uterorenal reflex, redistributing renal blood flow from cortex to medulla, activating the renin-angiotensin system, resulting in hypertension, and, proteinuria. Delivery of the baby relieves the "stretch" leading to immediate resolution of the pre-eclamptic syndromes. Exposing pregnant women to sustained levels of hypertension may injure renal vasomotor nerves contributing to early-onset (aged 40-50) hypertension and cardiovascular events following pregnancies complicated by pre-eclampsia. Exposing babies to sustained hypertension in utero may cause injuries to their kidneys resulting in childhood hypertension and its sequelae.

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Section: Postpartum Hypertensionmentioning

confidence: 55%

Pre-eclampsia: the uterine denervation view. Injuries to uterine nerves, the uterorenal “reflex”, and, renal cortico-medullary shunt

Yang¹,

Xin²,

Qing³

et al. 2019

Clin Obstet Gynecol Reprod Med

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“…The uterus and kidneys are supplied from the same sympathetic segments (T10-L2) so that any injury to the innervation to the uterus, may also result in injury to the innervation of the kidney including its vasomotor nerves. We already know that widespread visceral arteriolar narrowing in hypertension [39] arises from injuries to vasomotor nerves resulting from stress, hyperglycemia and persistent physical efforts during defecation [40,41].…”

Section: Hypertension and Coronary Artery Diseasementioning

confidence: 99%

“Endometriosis”: A neuro-etiologic framework for its causes and consequences

Xin¹,

Hao²,

Lan³

et al. 2019

Clin Obstet Gynecol Reprod Med

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In recent decades the gynecologic response to "endometriosis" has been to excise, or ablate, its deposits with high rates of recurrent pain. However, there is growing dissatisfaction with surgical outcomes, and, a chorus of clinicians recently called for an improved clinical approach. They want to enhance the use of "clinical" diagnosis to improve "delays in diagnosis", "bring about more rapid relief ", "limit disease progression" and "prevent sequelae". This ambitious agenda is not just a "call to action"; it implies a fundamental shift in approach -though the details of that "shift" were not detailed in the article.In the "autonomic denervation" view of the pathogenesis of "endometriosis", there are two key pathogenic principles that govern its laparoscopic appearances. Firstly, injuries to uterotubal nerves result in uterotubal dysmotility and retrograde menstruation with, ectopic endometrium deposited in the pelvis. "Difficult", first labors, straining on the toilet and gynecologic surgery cause the initial pelvic neural injuries. Secondly, ectopic endometrium attaches to anatomic sites of tissue injury e.g. injured uterosacral ligaments, injured peritoneal surfaces, hip replacements, etc if endometrium is available at the time of the injury. Breast feeding mothers do not have "available" endometrium. "Endometriosis" with accompanying injuries to pelvic autonomic nerves, may result in a surprisingly wide range of clinical consequences. These include "pain in response to light touch", sensitization of central nervous system, hyperplasia of the endometrium and myometrium, and, narrowing of adjacent myometrial arterioles resulting in pregnancy complications. Concurrent, or contiguous, injuries at other levels of the sympathetic chain may result in hypertension, inflammatory bowel disease, thyroid dysfunction, Sjogren's syndrome and other "autoimmune" diseases.Re-framing the condition as an injury to pelvic autonomic nerves with widespread, neurologic consequences consequences, may be a more appropriate, clinical framework than attributing such wide-ranging symptoms to isolated deposits of "ectopic endometrium"?

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The arteriolar injury in hypertension

Cited by 2 publications

References 9 publications

Pre-eclampsia: the uterine denervation view. Injuries to uterine nerves, the uterorenal “reflex”, and, renal cortico-medullary shunt

Pre-eclampsia: the uterine denervation view. Injuries to uterine nerves, the uterorenal “reflex”, and, renal cortico-medullary shunt

“Endometriosis”: A neuro-etiologic framework for its causes and consequences

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